History of Lyme & Testing

Antibody tests

Testing for the presence of B. burgdorferi antibodies used an
ELISA (enzyme-linked immunosorbent assay) that detects IgG
and IgM antibodies. The results of this test were available within
one day in 70% of cases and within three days in 88% of cases.
The total number of tests that were positive in the last three
years was 78. As the laboratory serves a number of different
hospitals and many patients were tested more than once, this case
series includes the majority of patients with a positive Lyme
antibody test.
Positive and equivocal samples on the immunoassay were sent
to the Lyme Borreliosis Diagnostic Unit of the Health Protection
Agency at Southampton, where immunoblots are performed to
assess reactivity to a range of B. burgdorferi antigens.

In this cohort, Lyme antibodies were tested for in 64 out of 65
patients with the screening ELISA; this was positive in 28 and
equivocal in eight. Immunoblots on both the ELISA positive and
equivocal samples were all positive at the reference laboratory.
ELISA was negative in 25 patients. Eleven ELISA negative blood
samples from patients thought to have the infection clinically
were sent to the reference laboratory at the specific request of
the responsible clinician, and six of these had positive
immunoblots. Overall 44 out of 64 patients had Lyme disease
serologically confirmed on immunoblot.

Source-http://lymeaware.free.fr/lyme/Diagnostiques/Lyme%20UK%20O’Connell.pdf
Chronic Lyme Post-Mortem Study Needed
Editorial by Tom Grier:
Key Words:
•Antibody: A protein produced by a white-blood-cell to attack
bacteria and viruses.
•Titer: Another word for level, as in level or amount of antibody
measured in the blood.
•Seronegative: Despite an infection there is an absence of
antibodies in the blood or serum of the patient.
•Spirochete: A spiral bacteria in the same family of bacteria as
Syphilis.
•Borrelia burgdorferi: The spirochete bacteria that causes Lyme
disease.
•Erythema Migrans: A red expanding rash on the skin caused by an
infected tick bite. An EM rash is diagnostic for Lyme disease even
in absence of a positive test.
•Antigen: Refers to a foreign substance in our blood that is
capable of causing an immune response.
There isn’t a disease in the past 100 years that has polarized the
medical community more than Lyme disease. From the very beginning,
it was misunderstood. In the early 1970’s, two concerned mothers,
Polly Murray and Judith Mensch, were convinced that the epidemic of
juvenile rheumatoid arthritis (JRA) cases they were seeing in their
neighborhoods in Old Lyme, Connecticut, were being contracted as a
result of some kind of environmental exposure rather than a genetic
disorder. After the state health department admitted that the JRA
incidence rate in that area was at least eight times the national
average, they somewhat reluctantly decided to investigate the
observations of these two woman. Murray and Mensch had to present
actual patient case histories they had collected before an
investigation was started.
In 1975, a rheumatologist named Dr. Alan Steere first described in
medical literature these abnormal cases of JRA as a new type of
arthritic disorder. He coined the term “Lyme Arthritis”. This led
to an immediate misunderstanding of Lyme disease, which was
incorrectly thought of as strictly an arthritic disease for many
years.
Six years later, in 1981, the actual cause of Lyme disease was
discovered to be a new species of spirochetal bacteria transmitted
to humans from the bite of infected deer ticks. Almost ten years
after Steere’s description of Lyme disease as an arthritic
disorder, it was now becoming recognized that Lyme disease was in
fact much more than just a new type of arthritis. Lyme disease was
now recognized as being equally capable of causing severe and
devastating neurological disorders. [Pachner AR, Steere AC. The
triad of neurologic manifestations of Lyme Disease: Meningitis,
cranial neuritis, and radiculoneuritis. Neurology 1985;35:47-53]
Dr. Willy Burgdorfer was the first to isolate the spirochetal
bacteria from the midgut of Ixodes Scapularis (deer ticks) gathered
from the Shelter Island area, located near the coast of New York
and New Jersey.
Shortly after the cause of “Lyme Arthritis” was discovered to be a
bacteria, articles appearing in medical literature quickly assumed
that the Lyme spirochete was similar to other bacterial infections.
Many treatment studies based their protocols of antibiotic
treatment on other bacterial infections, such as strep throat. The
conclusions from most early studies having short patient follow-up
concluded that you could expect Lyme disease to respond to 10-14
days of antibiotics. The antibiotics tested in the test tube and
deemed to be effective at that time included erythromycin,
tetracycline, and penicillin.
From the very beginning, treatment failures were seen in virtually
every antibiotic study done. The longer the patient follow up, the
higher the incidence of treatment failure. The medical community
blamed early treatment failures on the older antibiotics
erythromycin, tetracycline, and penicillin, and determined that
these antibiotics were not very effective at curing Lyme disease.
Ignored was the fact that the newer antibiotics were also
consistently failing to prevent relapses of active infection. Since
these early treatment studies, the concept that two weeks of
antibiotic therapy is adequate treatment for Lyme disease has
remained ingrained in the medical community’s collective
consciousness. [The Long-Term Follow-up of Lyme Disease: A
Population-Based Retrospective Cohort Study. Authors: Shadick NA;
Phillips CB; Sangha O et al. Ann Intern Med 1999 Dec
21;131(12):919-26]
*Data presented by Dr. Nancy Shadick at an International Lyme
Symposia showed that patients in the Nantucket Island study
followed for up to 5.2 years after initial antibiotic treatment had
ever-climbing relapse rates. Relapse rates in patients receiving
two weeks of IV Rocephin (ceftriaxone) could expect a relapse rate
to exceed 50% after five years.
Other factors that contribute to relapse post-treatment seem to
include length of infection before diagnosis, choice of antibiotic,
and severity of symptoms at time of evaluation.
While from the very beginning there have been thousands of patients
who have complained of still being sick and symptomatic despite
supposed adequate antibiotic treatments, most of the medical
community has ignored the patient’s observations and labeled them
as being cured – despite the fact that they still have most of the
same symptoms that brought them to their doctors in the first
place. So, what determines a cure if the patient still has the
symptoms of the disease? In many cases, it is not the patient’s
disability that determines the disease state, but rather the
presence or absence of natural immune factors or antibodies. The
problem is that antibodies are not a direct measurement of active
infection.
How could this have happened? Part of the problem was the newly
emerging science and technology of antibody serology testing known
as ELISA tests (Enzyme-Linked Immunosorbent Assay).
[ELISA tests look for an enzymatic color change that indicates the
presence or absence of Lyme antibodies in a patient’s serum. If you
still see a color change when a patient’s serum is diluted with 512
parts water, then it is said a patient has a dilution titer of
1:512. Note: Higher titer numbers do not have any correlation to
how sick a patient is feeling. In fact, a high number indicates the
presence of lots of immunity. A patient with a high titer is better
able to fight the infection than someone who is producing low
numbers of antibody or has a borderline or even negative titer.]
Not only was it clear that ELISA tests were quick and easy to
develop, but they were cheap and easy to administer. The
convenience of ELISA tests was a powerful enticement to both
doctors and patients. Let’s face it, taking a 10 cc vial of blood
is more convenient and inexpensive than having several brain, skin,
bladder, or heart biopsies costing thousands of dollars done. The
problem from the very beginning was that it was assumed and
generally accepted these tests were a better diagnostic tool than
patient evaluations based on symptoms and a response to treatment.
It was erroneously accepted that absence of antibodies in the blood
meant no infection was present anywhere in the patient’s body. Even
more disturbing was the incorrect assumption that the drop in
antibody levels during treatment indicated a microbiological cure.
Thus, many studies concluded that patients were cured if they
eventually tested negative for Lyme antibodies. Both assumptions
were and continue to be incorrect.
On paper, it certainly looks good for a doctor if he can tell a
patient that, based on the test, they are negative for Lyme
disease. However, in reality a more accurate statement would be
that the patient is simply negative for the presence of those
antibodies for which that particular test is sensitive for. Absence
of antibodies does not mean the patient cannot have active
infection.
ELISA tests can vary greatly from lab to lab. Since each lab holds
a patent on their particular test, they are all competing to say
they have the best test. It is a competitive business and certain
buzz words, such as specificity, sensitivity, efficacy, and
accuracy, are used to try to outsell one’s competitors lab tests.
This gives rise to many methods of testing efficacy implemented by
competing labs in order to say that their test is better than the
competition’s. This is usually based on predetermined laboratory
standards. Unfortunately, laboratory methods of determining an
ELISA test’s efficacy and accuracy does not directly correlate to
accuracy in determining infection in a human being.
If a laboratory tests its’ ELISA on 100 test tubes of an identical
known sample and, simultaneously, on 100 test tubes of distilled
water (the control group), and picks up 99 of the 100 samples and
only one of the control samples, they can claim their test is 99%
accurate. It had a 1% rate of false negatives and a 1% rate of
false positives. (The lab chooses what dilution titer it accepts as
positive. For one lab it maybe 1:256, while for another it may be
as high as 1:1024)
A 99% sensitivity sounds great, and most doctors and lay people
would determine that this ELISA test is 99% effective and accurate.
But these tests cannot tell you if a patient who is infected but
makes no antibodies (seronegative patients) has active Lyme
disease. Also, there is evidence that in humans with high titers,
the tests can still be as high as 55% inaccurate.
What if I told you that some manufacturer’s tests are sensitive to
only one of the antibodies we produce to the Lyme bacteria, and it
is an antibody that is rarely elevated in late Lyme? What if I told
you this test only had moderate sensitivity and requires highly
positive serum to have a reagent color change? What if I told you
that out of over 100 different Lyme ELISA tests by different labs,
each was slightly different? What would you think if I told you
that each lab holding a patent on an ELISA test presents data in
such a way to make their test appear to look better than the
competition in order to increase their profit? And, what would you
say if I told you that many medical institutions are actually
corporations that own patents on these Lyme tests, and that the
reputations of these institutions and the researchers who developed
them are all on the line if their test is found to be fallible?
What are the consequences to the reputations of these institutions
if patient who say they are still sick after treatment are denied
treatment because of these fallible tests? What if a patient
becomes disabled or dies? The admission that the Lyme bacteria is
alive and sequestered in some seronegative patients is not welcome
news to the developers of these tests. But, rather than do the type
of autopsy and tissue studies that would truly compare these tests,
the manufacturers have chosen to manufacture patient studies that
compare their tests to other equally bad serum tests. If a
carpenter has a yard stick 29 inches long and he tests its
precision with another yardstick 29 inches long, it will always
appear that his yardstick is accurate.
How do laboratory claims to the efficacy of these tests actually
stand up in the real world for the diagnosis of Lyme disease?
Hundreds of labs and ELISA tests were evaluated by independent
sources and were found several times to be less that 65% accurate.
(This was based on triple-paired identical positive serum samples
that were sent to 516 labs across the United States.) In some
cases, some labs were far below this average. Without even arguing
that some Lyme patient’s blood can be antibody negative despite an
active infection, the patient whose blood is highly positive runs
as much as a 45% chance or higher of still testing negative with an
ELISA test. So they can have loads of antibody and still test
negative simply by virtue of the lab’s inability to deliver
consistently accurate results.
Now consider this. By today’s diagnostic criteria, if you test
negative by ELISA, you don’t have Lyme disease. But, if you do test
positive, you still do not have Lyme disease until you also test
positive by Western Blot. A recent study shows that the Western
Blot can be less than 50% accurate. So, statistically, if the ELISA
test is 65% accurate and a Western Blot is 50% accurate,
multiplying these probabilities gives less than a 33% chance of
testing positive using the two tiered testing approach.
The biggest problem for Lyme patients today is that the medical
community still by and large makes the same two incorrect
assumptions about blood-based testing. This includes the more
recent PCR DNA blood tests, which have the same pitfalls as
antibody serologies in that the absence of infection of the
bloodstream does not mean absence of infection in the body. Two
important points to remember about antibody and PCR testing are: 1)
The absence of antibody (or bacterial DNA) does not prove absence
of infection and 2) the drop in antibodies (or the absence of Bb
DNA) does not guarantee that a patient is cured or that the patient
won’t relapse from active infection.
Example: Let’s consider that antibodies or bacterial DNA in the
patient’s serum are like hailstones you see during a hailstorm.
Standing in your yard with a five-gallon pail for several seconds,
you don’t collect a single hailstone. What can you conclude? The
absence of hail stones in your small bucket doesn’t exclude the
fact that it could have been hailing in your yard. You can use a
larger bucket and increase your odds, but what if the hailstorm is
just in one corner of your yard? Likewise, a small 10 cc vial of
blood may be inadequate to find an infection that isn’t even in the
blood.
A very important observation is that there is a history in medical
literature of symptomatic seronegative Lyme patients who have
received aggressive long-term antibiotic therapy and still have
been culture positive for active infection post-therapy. Tests can
be and are fallible, and infection can persist despite lengthy and
aggressive antibiotic therapy.
Other persistent infection studies have shown the presence of
Borrelia burgdorferi antigens, bacterial particles, bacterial
DNA/RNA, and the presence of the bacteria in tissue biopsies of
patients despite antibiotic therapy. Using staining techniques that
are sensitive for spirochetes, researchers have found the bacteria
in tissue biopsies from living patients as well as sequestered in
patient’s tissues at autopsy. All of these methods are a much more
direct measurement of the presence of Lyme bacteria than antibody
blood tests. But they are impractical tests for the average doctor
to perform on a daily basis.
•Why can infection be present in the body without the immune system
making measurable antibodies? Once an infection has left the
bloodstream, a patient may not make enough antibodies to test
positive. Once the infection has found a safer place in the body to
hide, it can avoid the immune system and also avoid any antibiotics
that are mainly circulating in the blood. Here is a list of
mechanisms of immune escape:
•Bb can be coated by human blocking antibody and become invisible
to killer immune cells.
•Bb can coat it self with B-cell membrane and cloak itself in human
proteins.
•Bb can find places like inside joints and tendons where it is
sequestered from the immune system and even antibiotics.
•Bb can go metabolically inactive.
•Bb can hide in the brain, heart, bladder, and possibly skin cells.
It is motile so it seeks out survivable places.
•Bb may have another form that lacks cell wall and therefore lacks
many of the antigens the human immune system would use to attack.
•Bb may hide inside some human cells.
Without infection being in constant contact with the blood-borne
immune system, the body shuts off antibody production. Antibody
levels will fall despite the fact that the infection is still
sequestered deep in the body, such as the brain, tendons, heart,
nerves, bladder, eyes, and joints. How do we know this? Patients
who have been repeatedly seronegative for antibodies have been
culture positive for the Lyme bacteria. Patients who have been
aggressively treated with antibiotics have been culture positive
for the Lyme bacteria. Despite repeated negative Lyme antibody
tests, these patients still had symptoms – symptoms that, in most
cases, responded to extended antibiotic therapies. [See references]
Because the medical community has by and large refused to accept a
patient’s symptoms as proof of infection and have continually based
their diagnosis of Lyme disease on Lyme serologies, there has been
an ever growing schism between so called “chronic Lyme patients”
and a medical community that refuses to accept their claims of
still having active infection post-treatment. In many cases, not
only are serologies used to determine the diagnosis, but the drop
in antibodies is often used to indicate a biological cure.
It has been the variable nature of the disease and its’ wide range
of symptoms, and the reliance on unreliable tests that has given
rise to two different camps concerning the diagnosis and treatment
of Lyme disease. Let’s discuss the evolution of these two opposed
paradigms of diagnosis and treatment in the next section.
The Need For A Post-Mortem Lyme Study
The medical community is unevenly divided into two opposing camps
on three major issues concerning Lyme Disease:
•What constitutes a proper diagnosis of Lyme disease?
•What constitutes proper treatment for patients with Lyme disease
who have symptoms that persist beyond four weeks of antibiotic
therapy?
•What role should Lyme tests play in both diagnosis and treatment?
The first camp on the diagnosis and treatment of Lyme disease:
The first camp, which I will call Camp A, represents the majority
of the medical community and is spearheaded by researchers from
Yale Medical, the American College of Physicians (ACP), and several
other major medical institutions. In general terms, this camp
believes that Lyme disease is best diagnosed through the use of two
consecutive serology tests; the ELISA test followed by a confirming
Western Blot. This is known as two-tiered testing. With very little
opposition from the medical community, two-tiered testing has now
become the diagnostic standard of most major medical centers.
Camp A also maintains that Lyme disease, despite the stage or
severity, is usually cured with just a few weeks of oral
antibiotics. This is by far the most popular position within the
medical community and the health insurance industry at this time.
How does Camp A make a diagnosis of Lyme Disease?
In the past, a history of a tick bite followed by a bull’s-eye skin
rash or erythema migrans rash was diagnostic of the disease, but a
diagnosis based on the rash and symptoms alone has come under
increasing attack by several advocates of two-tiered testing,
including Yale Medical [See Yale Medical Report] and the ACP.
A video training tape by the ACP is quite explicit that, in the
absence of an erythema migrans (EM) rash, the diagnosis must be
made by dual serologies and more than two weeks of antibiotics is
almost always unnecessary. In one of the video scenarios, the tape
suggests to treating physicians that patients who insist that they
have persistent symptoms post-treatment should be referred to
psychiatrists. The logic of this psychiatric referral stems from
the premise that, since antibiotics are accepted as curative, any
persistence of symptoms has to be purely psychological. So if a
patient doesn’t feel better post-treatment, send them to a shrink!
The second camp on the diagnosis and treatment of Lyme disease:
The second camp, often referred to as “Lyme advocates,” which I
will call Camp B, believes that most of the persistent symptoms
post-antibiotic treatment are caused by persistent infection. This
camp maintains that antibody serologies are poor at detecting a
spirochetal bacterial infection that has sequestered in deep
tissues and is no longer found within the bloodstream. They believe
spirochetes that have found sequestered, or privileged, sites tend
to hide in the body and are poorly detected by any means. As proof
of their position, this camp offers numerous studies which have
shown persistence of Borrelia infection post-antibiotic treatment.
Listed below are several of these published cases of persistent
infection in humans and animals post-treatment as confirmed by
either culture or tissue biopsy and stain:
•Schmidli J, Hunzicker T, Moesli P, et al, Cultivation of Bb from
joint fluid three months after treatment of facial palsy due to
Lyme Borreliosis. J Infect Dis 1988;158:905-906
•Liegner KB, Shapiro JR, Ramsey D, Halperin AJ, Hogrefe W, and Kong
L. Recurrent erythema migrans despite extended antibiotic treatment
with minocycline in a patient with persisting Borrelia burgdorferi
infection. J. American Acad Dermatol. 1993;28:312-314
•Waniek C, Prohovnik I, Kaufman MA. Rapid progressive frontal type
dementia and death with subcortical degeneration associated with
Lyme disease. A biopsy confirmed presence of Borrelia burgdorferi
post-mortem. A case report/abstract/poster presentation. LDF state
of the art conference with emphasis on neurological Lyme. April
1994, Stamford, CT*
•Lawrence C, Lipton RB, Lowy FD, and Coyle PK. Seronegative Chronic
Relapsing Neuroborreliosis. European Neurology. 1995;35(2):113-117
•Cleveland CP, Dennler PS, Durray PH. Recurrence of Lyme disease
presenting as a chest wall mass: Borrelia burgdorferi was present
despite five months of IV ceftriaxone 2g, and three months of oral
cefixime 400 mg BID. The presence of Borrelia burgdorferi confirmed
by biopsy and culture. Poster presentation LDF International
Conference on Lyme Disease research, Stamford, CT, April 1992 *
•Haupl T, Hahn G, Rittig M, Krause A, Schoerner C, Schonnherr U,
Kalden JR and Burmester GR: Persistence of Borrelia burgdorferi in
ligamentous tissue from a patient with chronic Lyme Borreliosis.
Arthritis and Rheum 1993;36:1621-1626
•Lavoie Paul E MD. Protocol from Rakel’s: Explains persistence of
infection despite “standard” courses of antibiotics. Lyme
Times-Lyme Disease Resource Center 1992;2(2): 25-27 Reprinted from
Conn’s Current Therapy 1991
•Masters EJ, Lynxwiler P, Rawlings J. Spirochetemia after
continuous high dose oral amoxicillin therapy. Infect Dis Clin
Practice 1994;3:207-208
•Pal GS, Baker JT, Wright DJM. Penicillin resistant Borrelia
encephalitis responding to cefotaxime. Lancet I (1988) 50-51
•Preac-Mursic V, Wilske B, Schierz G, et al. Repeated isolation of
spirochetes from the cerebrospinal fluid of a patient with
meningoradiculitis Bannwarth’ Syndrome. Eur J Clin Microbiol
1984;3:564-565
•Preac-Mursic V, Weber K, Pfister HW, Wilske B, Gross B, Baumann A,
and Prokop J. Survival of Borrelia burgdorferi in antibiotically
treated patients with Lyme Borreliosis Infection 1989;17:335-339
•Georgilis K, Peacocke M, and Klempner MS. Fibroblasts protect the
Lyme Disease spirochete, Borrelia burgdorferi from ceftriaxone in
vitro. J. Infect Dis 1992;166:440-444
•Haupl TH, Krause A, Bittig M. Persistence of Borrelia burgdorferi
in chronic Lyme Disease: altered immune regulation or evasion into
immunologically privileged sites? Abstract 149 Fifth International
Conference on Lyme Borreliosis, Arlington, VA, 1992 *
•Lavoie Paul E. Failure of published antibiotic regimens in Lyme
borreliosis: Observations on prolonged oral therapy. Abstract
presented at the 1990 Lyme Borreliosis International Conference in
Sweden.*
•Fried Martin D, Durray P. Gastrointestinal Disease in Children
with Persistent Lyme Disease: Spirochetes isolated from the G.I.
tract . 1996 LDF Lyme Conference Boston, MA, Abstract*
•Neuroboreliosis: In the journal Annals of Neurology Vol. 38, No 4,
1995, there was a brief article by Dr. Andrew Pachner MD, Elizabeth
Delaney BS, and Tim O’Neill DVM, Ph.D. The conclusion of the
article was simple and concise: ” These data suggest that Lyme
neuroboreliosis represents persistent infection with B.
burgdorferi.” The study used nonhuman primates as a model for human
neuroborreliosis, and used a special PCR technique to detect the
presence of Borrelia DNA within specific structures of the brains
of five rhesus monkeys. The monkeys were injected with strain N40Br
of Borrelia burgdorferi, and later autopsied for analysis.
(For further information, please refer to the compendium of
references to the persistence or relapse of Lyme disease at
http://www.geocities.com/HotSprings/Oasi…)
Abstract summaries:
•Abstract # D654 – J. Nowakowski, et al. Culture-Confirmed
Treatment Failures of Cephalexin Therapy for Erythema Migrans. Two
of six patients biopsied had culture confirmed Borrelia burgdorferi
infections despite up to 21 days of cephalexin (500 mg TID)
antibiotic treatment. · Abstract # D655 – Nowakowski, et al,
Culture-confirmed infection and reinfection with Borrelia
burgdorferi. A patient, despite antibiotic therapy, had a recurring
Erythema Migrans rash on three separate occasions. On each occasion
it was biopsied, which revealed the active presence of Borrelia
burgdorferi on two separate occasions, indicating reinfection had
occurred.
•Abstract # D657 – J. Cimperman, F. Strle, et al, Repeated
Isolation of Borrelia burgdorferi from the cerebrospinal fluid
(CSF) of two patients treated for Lyme neuroborreliosis. Patient
One was a twenty year old woman who presented with meningitis but
was seronegative for Borrelia burgdorferi. Subsequently, six weeks
later Bb was cultured from her CSF and she was treated with IV
Rocephin 2 grams a day for 14 days. Three months later, the
symptoms returned and Bb was once again isolated from the CSF.
Patient 2 was a 51 year old female who developed an EM rash after
tick bite. Within two months she had severe neurological symptoms.
Her serology was negative. She was denied treatment until her CSF
was culture positive nine months post-tick bite. She was treated
with 2 grams of Rocephin for 14 days. Two months post-antibiotic
treatment, Bb was once again cultured from her CSF. In both of
these cases, the patients had negative antibodies but were culture
positive, suggesting that the antibody tests are not reliable
predictors of neurological Lyme Disease. Also, standard treatment
regimens are insufficient when infection of the CNS is established
and Bb can survive in the brain despite intravenous antibiotic
treatment.
•Patients with ACA shed Bb DNA post-treatment: Aberer E. et al.
Success and Failure in the treatment of acrodermatitis chronica
atrophicans skin rash. Infection 24(1):85-87 1996. ACA is a late
stage skin rash usually attributed to Borrelia afzelii, it is
sometimes mistaken for scleroderma. Forty-six patients with ACA
were treated with either 14 days of IV Rocephin or thirty days of
oral penicillin or doxycycline and followed up for one year. Of
those treated with IV, 28% had no improvement, and 40% still shed
Bb antigen in their urine. Of the oral group, 70% required
retreatment. Conclusion: Proper length of treatment for ACA has yet
to be determined.
•Logigian EL, McHugh GL, Antibiotics for Early Lyme Disease May
Prevent Full Seroconversion but not CNS Infection. 1997 ABSTRACT #
S66.006 Neuloogy Symposia, NEUROLOGY 1997; A388:48 In this study,
22 late-stage neurological patients who met the Centers for Disease
Control (CDC) criteria for Lyme disease were studied over a three
year period. Eighty-five percent of seronegative patients who still
had active disseminated infection had been treated within one month
of tick bite. This means that early antibiotic treatment may make
you test negative, but you still progress to develop encephalitis.
Without antibodies your brain has no natural immunity or local
immune system to fight the infection, so withdrawing antibiotics
causes the infection in the central nervous system (CNS) to go
unabated. Patients who go on to develop brain infections despite
antibiotics, may have suppressed antibody production thus worsening
any remaing active infection in the central nervous system.
•Valesova H, Mailer J, et al. Arthritis: A three year follow-up:
Long-term results in patients with Lyme disease followed for three
years after two weeks of IV Rocephin. Infection 24(1):98-102, 1996.
This study represents another of the problems with author’s bias
interpretation of data. Thirty-five Lyme arthritis patients were
treated with a two week course of IV Rocephin. They were then
followed for three years. At the end of the study, six patients had
complete relapses, nineteen had marked improvement, four had new
Lyme symptoms, and the rest were lost to follow up. The authors
conclusion: ” The treatment results for this group of 35 Lyme
arthritis patients are considered successful.”
Let’s look at the above figures mathematically, based on the 29
patients out of 35 who were contacted and assessed:
•19 improved = 65 %
•6 relapsed = 20 %
•4 worsened = 15 %
Does a total of 35% of patients still suffering sound like
successful treatment to you? This is a treatable disease, but you
have to treat it! What if a doctor’s child was one of the 35%? Do
you think they would continue to go untreated as suggested by the
ACP? How many patients have to relapse before treatment is
considered unsuccessful? Six patients – or 20% – had complete
relapses, yet the conclusion of the study was that, in general,
treatment was considered successful! We get better cure rates for
tuberculosis.
Animal vs. Human Studies:
Support for the theory that Borrelia burgdorferi can find safe
havens in sequestered sites despite antibiotic therapy comes from
several animal model studies. However, only a few human cases have
yet been published. This is because the tissue studies that are
required almost demand that they be done in a post-mortem exam.
(See Stanek and Appel’s work on skin biopsies verses post-mortem
exam of deep tissues in Lyme infected and antibiotic treated
beagles)
Abstract # D607 – M.J.G. Appel, The persistence of Bb in Dogs after
antibiotic treatment. Seventeen Beagle puppies were infected with
Bb from infected ticks, eleven were treated for four weeks with
either Doxycycline or amoxicillin in doses according to weight. Six
were control dogs. 1/11 had Bb isolated from skin, but 7/11 dogs
had Bb isolated from other tissues during post-mortem. All of the
persistent infected pups had persistent arthritis. Conclusion: Skin
biopsies are not predictive of persistence of infection. Also the
standard excepted four week course of antibiotic treatment in dogs
is not sufficient.
To date, no major multi-center post-mortem Lyme disease study has
ever been done on humans. Without this type of post-mortem study,
the debate between the two disagreeing camps will almost certainly
continue.
Results from the European Alzheimers study done by Dr. Judit
Miklossy suggests that post-mortem exams should not only look for
persisting spirochetes in deceased Lyme patients, but should also
look for spirochetes in the brains of deceased dementia patients as
well.
•Miklossy J, Kuntzer T, Bogousslavsky J, et al. Meningovascular
form of neuroborreliosis: Similarities between neuropathological
findings in a case of Lyme disease and those occurring in tertiary
Neurosyphilis. Acta Neuro Pathol 1990;80:568-572
•Miklossy Judit. Alzheimer’s disease a spirochetosis? Neuro Report
1993;4:841-848 Thirteen out of thirteen Alzheimer patients had
spirochetes in the brain. None of the age-matched control subjects
had evidence of spirochetes in their brains. This study suggests
that there is a correlation between an Alzheimer’s dementia and CNS
spirochetosis in Swiss patients. In other words spirochetes might
contribute to a CNS dementia similar to Alzheimer’s disease. (This
is not to suggest that all Alzheimer’s is caused by spirochetes,
but even if a small percentage of dementia can be prevented by
antibiotics then further studies are justified. None are currently
being done! ?
To do this type of tissue study of sequestered spirochetal
infections takes nearly heroic efforts in time, costs, and
diligence. Yet the few times that these types of studies have been
applied to humans have suggested that Borrelia burgdorferi can
indeed survive and thrive within the human body despite a complete
course – or even several courses – of antibiotic therapy.
Yours sincerely,
J McCullough

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